Diets containing abundant sodium chloride lead to a drain of calcium from bone, the body's major calcium reserve, into the urine. In young men and women, this salt-induced loss of skeletal calcium leads to homeostatic adjustments of parathyroid and vitamin D activity that increase intestinal absorption of dietary calcium. This endocrinologic- gastrointestinal response appears to be impaired in older subjects. In postmenopausal women, therefore, chronic ingestion of abundant sodium chloride might lead to sustained uncompensated urinary calcium losses and abnormally high rates of bone resorption, and contribute to the pathogenesis of osteoporosis. Salt-induced urinary calcium losses and increases in bone resorption rate might be prevented by supplementation of the diet with potassium bicarbonate, an absorbable alkali salt with potent anti-calciuric properties. We will determine in postmenopausal women whether salt-induced hypercalciuria is truly associated with increased bone turnover, using highly specific modern biochemical markers of bone resorption and formation; whether the changes in bone turnover among subjects are predicted by the changes, or lack thereof, in the parahormone-vitamin D axis; and whether chronic supplementation of the diet with potassium bicarbonate can prevent salt-induced hypercalciuria and increased bone turnover. In this randomized, double- blinded, placebo-controlled study, postmenopausal women (n=50) will be first adapted to a low salt diet (70-90 meq/day) for three weeks then randomized to one of two treatment groups (n=25 subjects each): (a) high-salt diet (210-230 meq/day) with placebo, or (b) high-salt diet (210-230 meq/day) with added potassium bicarbonate (90 mmol/day) for four weeks. After each study period, urinary calcium, cyclic AMP, markers of bone resorption (deoxypyridinoline, N-telopeptide); and serum parathyroid hormone, calcitriol, and markers of bone formation (osteocalcin, type I collagen propeptide) will be measured. This study thus will determine in postmenopausal women whether dietary salt, as a hypercalciuric agent, stimulates bone resorption, to what extent that effect may be mitigated by endocrinologic homeostatic mechanisms, and whether chronic supplementation of the diet with potassium bicarbonate will prevent salt-induced hypercalciuria and increased bone resorption.